Among these, only adenosine can activate A2AR and promote the induction of Foxp3+ Treg cells,[16, 53] Given that Treg cells are the primary adenosine provider in the tumor microenvironment (TME), the upregulation of ectonucleotidases, CD73, and CD39 on Treg cells by GHCer may further fuel adenosine generation, creating a positive feedback loop that fosters GHCer‐induced immunosuppression. The gene discussed is FOXP3; the disease is neoplasm.